Acute pancreatitis clinical findings

Amylase enters the blood largely via the lymphatics. An increase in hydrostatic pressure in the pancreatic ducts leads to a fairly prompt rise in the amylase concentration of the blood. Neither an increase in volume flow of pancreatic juice nor stimulation of pancreatic enzyme production will cause an increase in senm enzyme concentration. Elevation of intraductal pressure is the important determinant. Stimulation of flow in the face of obstruction can, however, augment the entry of amylase into the blood, as can disruption of acinar cells and ducts. A functional pancreas must be present for the serum amylase to rise. Serum amylase determination is indicated in acute pancreatitis in patients with acute abdominal pain where the clinical findings are not typical of other diseases such as appendicitis, cholecystitis, peptic ulcer, vascular disease or intestinal obstruction. In acute pancreatitis, the serum amylase starts to rise within a few hours simultaneously with the onset of symptoms and remains elevated for 2 to 3 days after which it returns to normal. The peak level is reached within 24 hours. Absence of increase in serum amylase in first 24 hours after the onset of symptoms is evidence against a diagnosis of acute pancreatitis (76). 

Clinical assessment of severity in AP is still one of the most useful approaches. The accuracy of initial assessment on admission is about 40-68%, depending on the experience of the examining clinician (C7), and increases to 70-80% after 48 hr (H2). A study performed by Uhl et al. (U2) revealed no differences in the severity of acute pancreatitis caused by gallstones, alcohol, and other factors. The same findings were published by Lankisch et al. (LI). 

Once the presence of fasting lipemia has been established, di-ffereyitiation between primary and secondary hyperlipemias can usually be made on the basis of presence or absence of clinical and laboratory findings characteristic of an underlying disease. Plasma lipid and lipoprotein patterns as determined by lipid analyses, ultracentrifugation and electrophoresis are not necessarily diagnostic since similar findings are present in EHL and hyperlipemia of diabetic ketoacidosis, acute pancreatitis, alcoholism, etc. (Schettler 1955, Lees and Fredrickson 1964, Jahnke 1965). 

---